Thank you. I appreciate both the information and the caution.
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Is the injection pen as painless as ozempic?
I have been on Repatha for 4 months or so. That along with 10 MG of Rosuvastatin has had a dramatic effect on lowering my cholesterol. I haven’t experienced any negative side effects or injection site issues. The statin reduced my LDL-C to 79 and my ApoB to 80. But since I have high lp(a) I pushed for the PCSK9i. That reduced my LDL-C to 39 and my ApoB to 59 (LDL-P was 342). I wish I had started sooner.
The U-shaped curves are silly. I am lean with low visceral fat and so I have a low BMR. Because I am in the lowest quartile my all-cause mortality risk is 3 to 4 times higher than people who are metabolically unhealthy. It’s the same thing with cholesterol. You are lumped together with people who are frail, malnourished, suffering from chronic diseases or cancer. And yes, they die at much higher rates. But if you have a low BMR because you’re metabolically healthy or you have low cholesterol, thanks to lipid lowering drugs, then you have nothing in common with them.
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I’ve been on repatha for several years. I can’t compare it to the ozempic pen, but it only hurt a bit a handful of times. Normally it’s not a big deal and at most it might just be a quick slight ouch. Nothing to avoid it over.
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Agree hardly any pain, probably less than putting on a CGM
"The incredible shrinking stomach’
A little weekend diatribe…
I don’t like to get into the subject of dietary weight loss programs, PCSK9 inhibitors, etc., and even less on the pros and cons of vegetarian versus carnivore diets.
But here is what I know from personal experience and study of the subject of weight loss:
Calories count, forget about the effect of exercise, etc. If you want to lose weight you have to reduce caloric intake.
Calorie restriction is still the most proven method of extending lifespan in all animals.
The key is shrinking stomach size. If you are overweight the first thing you need to do to achieve long-term goals of CR without hunger etc. is to decrease stomach size.
Yes, I know many people have a problem achieving this, because of hunger, etc.
Though I must interject. IMO: It is easier to avoid hunger and reduce stomach size on low-carb diets.
To do this you need to stop stretching your stomach. Instead of big meals eat more smaller meals. You can do this by following an old yoga adage “Only eat when you are hungry.”
This works eventually even if you are a “stress eater”. i.e. eating food is a comfort for you.
Then eat slowly enough so your system has time to signal the brain that you are no longer hungry. Don’t stretch your stomach with large amounts of liquids.
Smaller more frequent meals and smaller more frequent liquid intake is the key to shrinking your stomach. The smaller your stomach the easier it is to satisfy your hunger.
This is not a short-term process, it may take weeks or months to achieve. This works whether or not you are on keto or some other diet.
“Portion Control: Eating smaller, more frequent meals can help reduce the stomach’s capacity over time. The stomach is a flexible organ that can adapt to smaller food volumes.”
“When the stomach is smaller, it fills up more quickly with less food, sending signals of fullness to the brain sooner.”
“Reduced stomach size can also affect the production of hunger hormones like ghrelin, leading to decreased appetite.”
The result is this: You will eventually become used to smaller meals. This is achieved without ever having to go hungry.
I have achieved a BMI of less than 22 for almost three years. Currently, I am sitting around 21. I went from 237 lbs to 172 lbs without too much effort, mostly just following various interventions that did not require me to be hungry.
Determining what CR is needed according to age activity, etc., is not an exact science. But, according to various online calculators, my CR is between 10 -20 percent.
I have achieved weight stasis. All lipid and glucose levels are well within the “normal range”.
I am experiencing no detectable sarcopenia, and I am never hungry. I eat just enough to maintain my current body weight. Because of my age, I eat a low-carb, protein-heavy diet.
I do 18/6 two meals a day. I never eat after 6 pm.
Bottom line:
If you ever want to achieve CR without hunger, you must shrink your stomach.
I am 83, and today, I feel like I will at least reach 100 while still being independent.
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Yes, I resemble that remark. Repatha and in the Horizon (Pelecarsen) study too. Not dead yet, so perhaps I’m not in the control arm!
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My experience with repatha over the past 2 months has been fairly underwhelming I’d say. Zetia and a < 30g saturated fat diet put my ApoB in the 80-100 range from 120-180. Bempedoic acid further reduced it to 54-64 range. Adding Repatha moved it to 43-46 range. My aim was to get down to the 30-40 range given my Lp(a) and family heart disease history. Perhaps it will lower a bit more in a month or so, but a 10 point reduction feels underwhelming given that some people on repatha monotherapy seem to get down to 30-50.
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I would wait 6 months and do labs before you decide to discontinue treatment.
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N=1 I have had nofun with Repatha. Severe cough developed. Switched to Inclisiran (6month pcsk9i) -severe brain fog and muscle weakness. now at 8m post injection starting to feel normal. Bemp.Acid arrives tommorow and will give that a whirl. Fingers crossed as I have tried all the other statins and ezetimibe( effective but muscle weakness brain fog and urticaria )
Sorry to hear that. I am repatha and do fine, but I started off praluent, so I wondered if you have tried that one to see how you respond?
Update, now LDL is 26 and ApoB < 35, I guess that’s labcorp’s detection limit. Repatha + Bempedoic Acid + Zetia. Lab taken ~2 days before my next dose (taken every 2 weeks).
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Great result, well done for sticking with it.
Just out of interest do you know whether Repatha has impacted your Lp(a) at all?
I forgot to have Lp(a) tested again. Will check in a month or so and report back.
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https://pubmed.ncbi.nlm.nih.gov/31714636/
Models for HMGCR, APOB, and NPC1L1 did not suggest that the use of related lipid-lowering drug classes would affect AD risk. In contrast, genetically instrumented exposure to PCSK9 inhibitors was predicted to increase AD risk in both of the AD samples (combined odds ratio per standard deviation lower LDL-C inducible by the drug target = 1.45, 95% confidence interval = 1.23-1.69). This risk increase was opposite to, although more modest than, the degree of protection from coronary artery disease predicted by these same methods for PCSK9 inhibition.
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While the MR data presented here makes the association interesting, there are so many other possible explanations for this association that my tendency is to dismiss it until large scale analysis of individual snps directly associated with PCSK9 dysfunction are analyzed for AD risk.
From the discussion of this paper ( although probably a ver small number)
“Moreover, when considering SNPs with the greatest evidence of functional relevance in the PCSK9 region, such as the rare missense variant rs11591147, genotype–AD associations were on the side of higher risk per LDL‐lowering allele but were not statistically significant individually in either dataset or when meta‐analyzed.“
There are many discussions of the PCSK9i and AD connection with MR on this site. For example take this post and several after that one with pretty involved discussion:
FWIW, I don’t think the issue is settled. Nonetheless out of an abundance of caution I’m staying away from PCSK9i. Probably excessively paranoid, but I’m waiting for other drugs addressing ApoB/LDL.
There are some statistical concepts which explained it, John Kastelein from NewAmsterdam Pharma have written about this. Based on that it’s bunk.
Besides I think we need a mechanism of action, always, unless the experimental data is rigorous else we’re in the “coffee increase longevity” magazine discussions, which is fine and applicable but not the best. MR makes sense when there’s mechanistic feasibility to also avoid confounding factors during the analysis.
But anyway there’s not much suggesting they’re better than statins for someone who have no issues with them. I wouldn’t race after them in that case. Pitavastatin looks good. YMMV.
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PCSK9i have been around long enough that I think we are beyond MR in studying this. A good powered RCT should answer this question definitely if the association is strong.
I have taken them for a year. No side effects. My LDL averages 30 or less. I highly recommend them to keep your arteries healthy.
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